Rheumatoid Arthritis is a chronic autoimmune disease and a major cause of disability. Current treatment of arthritis involves administration of drugs mainly by oral and parenteral route. Frequent dosing often leads to patient non compliance. Accounting this problem, drug delivery technologies should be developed which reduces frequency of dosing along with sustained release of medicament. Various drug delivery systems are documented like albumin-based drug delivery systems, bio-reductive drug delivery systems, microspheres, nanoparticles, liposomes etc. Conventional drugs like indomethacin, magestrol acetate, methotrexate and cannabidiol have been modified into extended release formulations, nano crystal oral suspensions, topical gel and transdermal patch respectively. Targeting αγβ3 integrin has been shown to enhance drug delivery. Drugs delivered by intra-nasal route significantly reduce disease severity in experimental collagen induced arthritis model. This review reports a comprehensive overview of newly developed drug delivery technologies as therapeutic targets of rheumatoid arthritis which may potentially reduce adverse extra-articular side effects. Introduction Rheumatoid Arthritis (RA) is a chronic autoimmune disease of unknown etiology, characterized by joint synovial inflammation and progressive cartilage & bone destruction resulting in gradual immobility ( 1 ). It was first found in early Native American population several thousand years ago but might have appeared in Europe after 17 [[[th]]] century ( 2 ). Recent research has produced exciting information about pathogenesis of RA. It is suggestive that activated synovial fibroblast plays a major role in both initiating and driving RA in addition to macrophages and T cells ( 3 ). In RA there is significant difference between the superficial synovial fibroblast lining and deeper synovial fibroblast lining. Synovial fibroblast differs morphologically and biologically from normal synovial tissue. These morphological and biological changes of synovial fibroblast results from specific changes in transcriptional genes and intracellular signaling cascade. The transcription factor NF- kB is activated in RA and appears to be important for progression of disease as well as in mediating inflammation ( 4567 ). Various inducers and targets of NF-kB serves as a potential target for treating RA ( 8 ). (Table 1).
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